This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We have developed a technique to simulate the docking of the human immunodeficiency virus (HIV) with a cell membrane. The technique, called Brownian Adhesive Dynamics. includes the thermal motion of the virion (Brownian dynamics) coupled to a stochastic binding of the receptor and ligand (Adhesive Dynamics). Our simulation can be used to predict the number of bonding protein spikes in steady state viral docking as well as the effect of gp120 viral surface density on the probability of HIV binding. Previously, our models for gp120 have been simple, where we model gp120 as a single reactive spring. However, it is known that gp120 exists as a homotrimer, and that gp120 has multiple binding sites for the two receptors with which it binds CD4 and the chemokine receptor. To address these complexities, we have coarse-grained the gp120 molecule, making it a trimer, and modeling it as a Rouse polymer. Thus, the simulation now involves tracking the Brownian motion of a virus, simultaneously with tracking the Rouse dynamics of gp120 molecules on the viral surface, of which there may be as many as 72. We seek to calculate the relationship between the number of gp120 trimers, the density of cell surface receptors (both CD4 and chemokine receptors) and the probability of viral docking and entry into a wide variety of host cell types. We used our initial DAC allocation to determine the increase of computational time required to simulate the docking of a single virus. Our preliminary results indicate that small changes in the density of chemokine receptors on the cell surface have a large impact on the time before a virus can infect the cell. This result has implications on the efficacy of newly FDA approved entry inhibiting agents (enfuvirtide and maraviroc) against viral infection. We seek additional computational resources to conduct extensions of these these biologically-important simulations to determine whether increasing the density of the primary receptor (CD4) can compensate for low chemokine receptor density on the kinetics of viral infection.